I would like to add some research in answer to a paragraph in Dr Peter D'Adamo's discussion on Lectins and Mitogens in http://www.dadamo.com/science.htm
"How mitogens work is still imperfectly understood. Con-A has been shown to induce microtubule assembly in polymorphonuclear leukocytes. Lectins have been shown to cause early changes in cytoplasmic free Ca2+ and influence the lymphocyte membrane potential. Both Con-A and PHA were studied as to their effect on lymphocyte glycosyltransferase activty. The investigators found that this enzyme, associated with increased transport activity of sialic acids, galactose and NAG was stimulated by Con-A but not by PHA. Thus the mitogenic effects of lectins on lymphocytes is not constant."
The research of Brand and others found what really happens in mitogen- and antigen- stimulated cells. ConA and PHA are found in all eukaryotic cell membranes including bacteria. It was found that the amount of ATP produced by mitotic division was similar to the amount produced by mitochondria during non-mitotic cellular operations, i.e. the vegetative state of a cell up to the early "S"phase of the cell cycle. However, during mitosis there is a switch to a so called "aerobic glycolysis," i.e., without the involvement of mitochondrial aerobic respiration, where glucose is reduced to form pyruvate and lactate.
Brand's research group demonstrated that the switch from ROS (reactive oxygen species) formation of mitochondrial oxidative phosphorylation during the vegetative state to mitotic aerobic glycolytic gene expression is redox dependent. The former requiring oxidative signals and the latter requiring reductive signals. This switching of ATP production is one of the oldest effective strategies to minimise oxidative stress on proliferating cells.
Droge research group found that the mitochondrial DNA in ConA stimulated T lymphocytes were protected by the anti-oxidative sulfur molecules (thiols), cysteine and glutathione, and the addition of H2O2 which is neutralized by selenium-dependent enzyme, glutathione peroxidase, where oxidized glutathione is further reduced by glutathione reductase and NADPH. The author suggests that the deciding factor to switch to aerobic glycolysis may be a critical level reached in the thiol pool.
Brand K, Hermfisse U. Aerobic glycolysis by proliferating cells: a protective strategy against reactive oxygen species. http://www.ncbi.nlm.nih.gov/pubmed/9141507
Droge W, Eck HP, Mihm S. HIV-induced cysteine deficiency and T-cell dysfunction--a rationale for treatment with N-acetylcysteine. http://www.ncbi.nlm.nih.gov/pubmed/1378279